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Internal Medicine > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What test best assesses thyroid function

A

TSH

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2
Q

What will happen to TSH in primary/secondary hyperthyroidism and primary/secondary hypothyroidism

A

Primary hyperT->TSH low, negative feedB
Secondary hyperT->+TSH= +T3/T4
Primary hyperT: +TSH->less negative feedB
Secondary hypoT: TSH low/normal with variabl response to TRH depending on site of lesion

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3
Q

When should free T3 be measured and why

A

If TSH suppressed and free T4 normal to rule out T3 toxicosis

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4
Q

When are thyroglobulin antibodies, TPO antibodies and TSH receptor inhibiting antibodies found

A

Hashimotos

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5
Q

When are Thyroid stimulating antibodies positive

A

Grave’s

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6
Q

What is the role of plasma thyroglobulin monitoring

A

Used to monitor residual thyroid activity post thyroidectomy

Normal/elevated suggest persistent, recurrent or metastatic disease

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7
Q

When might calcitonin be measured

A

If suspect medullar carcinoma / Men 2a or 2b symptoms

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8
Q

What is the role of thyroid USS

A

Size
Cystic vs solid nodule
FNAB

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9
Q

When is technitium scan done

A

Test of structure-> if nodule and hyperthyroid with low TSH

Differentiates between hot and cold nodules

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10
Q

When is radioactive iodine used

A

Test of function->order if thyrotoxic
Turnover of iodine
+uptake= overactive
-ve uptake->gland is leaking, exogenous hormone use, excess iodine (amiodarone/contrast dye)

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11
Q

When is FNA done

A

Differentiates between benign and malignant

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12
Q

When is RAIU increased

A

Graves
TMG
Toxic adenoma

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13
Q

When is RAIU decreased

A

Subacute thyroiditis
Recent iodine load
Exogenous iodine hormone

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14
Q

Define thyrotoxicosis

A

Clinical, physiological and biochemical findings in response to elevate thyroid hormone

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15
Q

Etiology of thyrotoxicosis

A

Hyperthyroidism:
Graves
MNG
Toxic adenoma

Thyroiditis:
Subacute
Silent
Postpartum

Extrathyroidal:
Endogenous->struma ovarii, teratoma, metastatic follicular
Exogenous

Excessive thyroid stimulation:
Pituitary thyrotroph
Pituitary thyroid hormone receptor resistance
+hCG (pregnancy, -ve TSH, +T4)

Drugs:
Amiodarone
Lithium
Phenytoin
Carbamazepine
Rifampin
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16
Q

Clinical features of thyrotoxicosis

A

General: fatigue, heat intolerance, irritability, fine tremor
CVS: Tachy, AF, palpitations
GI: weight loss, diarrhea, +appetite, thirst, +frequency
Neurology: proximal myopathy, hypokalemic periodic paralysis
GU: oligomenorrhea, amenorrhea, decreased fertility
Dermatology: fine hair, moist, vitiligo, soft nails with onycholysis, palmar erythema. Acropachy and pretibial myxedema in Grave’s
MSK: decreased bone mass, muscle weak
Hematology: Graves->leukopenia, lymphocytosis, splenomegaly, lymphadenopathy
Eye: Graves->lid lar, retraction, proptosis, diplopia, decreased acuity, puffy, conjunctival injection

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17
Q

Overview management for thyrotoxicosis

A 
Propylthiouracil/Carbimazole
Propranolol
Radioiodine
Thyroidectomy
Get help in pregnancy and infancy
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18
Q

Triad of Grave’s

A

Hyperthyroidism
Infiltrative opthalmopathy
Pretibial myxedema

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19
Q

Pathogenesis of Graves->pituitary, heart, liver, bone, genital, metabolic, white fat, CNS, muscle

A

Thyroid stimulating hormone receptor antibodies (TSI)->triggering->mimics TSH->+growth of thyroid gland
Pituitary->-ve expression of thyrotropic= Suppressed TSH
Heart->+ANP=+rate/contractility
Liver->+T1deiodinase, LDL receptors= +peripheral T3, -ve LDL
Bone->+psteocalcin, +ALP= +bone turnover
Genital->+SHBG, -ve testosterone, estrogen antagonism=-ve libido/erection, irregular menses
Metabolic->+FA oxidation, +Na/K ATPase= +thermogenesis
MSK->+SRCa2+ activated ATPase= proximal myopathy

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20
Q

Key factors in Grave’s

A 
Risk factors
Heat intolerance
Sweating
Weight loss
Papitations
Tremor
TachyC
Diffuse goitre
Opthalmopathy
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21
Q

Investigations in Grave’s disease

A 
TSH (suppressed)
Free T4 (+, not in T3 toxicosis/subclinical)
Free T3
T3RU, Free T4 index
FBC (normocytic normochromic)
UEC, Ca+ LFT+
Thyroid autoantibodies
If opthalmopathy->visual acuity testing, eye movements

May consider: RAIU, TIS, T U/S (highly vascular, diffuse, enlarged)

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22
Q

Triggering events in Grave’s

A

Stress
Infection
Childbirth

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23
Q

What autoimmune conditions are associated with Grave’s

A

Vitiligo, T1DM, Addisons

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24
Q

What is the typical age of Grave’s patient

A

40-60 years

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25
Q

Initial management of Grave’s/hyperthyroidism

A

Carbimazole
Propranolol (usually only until rendered euthyroid)
DIltiazem (when CI to beta blockers)

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26
Q

When is dosing reassessed

A

Every 3-6 weeks

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27
Q

Is dosing initially based on TSH, or T3/T4 and why

A

TSH can be suppressed for months after hyperthyroidism is corrected

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28
Q

When is the maximum chance of remission for Grave’s

A

After 12-18 months of antithyroid medication

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29
Q

What are the options for subsequent therapy for hyperT

A

Continued antiT
Withdrawal
RI treatment
Thyroidectomy

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30
Q

When is surgery considered

A

Tracheal pbstruction/narrowing
Dysphagia
Stridor
Cosmetic

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31
Q

Preferred management in older people with large goitre

A

Antithyroid then RI

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32
Q

F/u after remission of hyperthyroidism

A

clinical and biochemical follow-up is at 1, 2, 3 and 6 months, then annually thereafter. The patient should be instructed to have prompt testing if any symptoms of recurrent hyperthyroidism develop.

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33
Q

Management of thyrotoxic storm

A 
ABC
2 large bore cannula
IVF
NGT if vomiting
Bloods for T3, T4, STH, cultures (if suspect infections)
Monitor BP
Sedate if necessary
Propylthiouracil
Lugol's solution
Dexamethasone
Propranolol
Adjust fluids, cool with tepid sponging, paracetamol
Get endocrinologist involved
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34
Q

Treatment of thyrotoxic storm overview

A
  1. Couteract peripheral effects
  2. Inhibit thyroid hormone synthesis
  3. Treat systemic complications
    Block hormone synthesis and release
    Decrease conversion of T4 to T3
    Control tachyC and rate dependent HF
    Restore hydration
    Give sedation if necessary
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35
Q

S&S thyrotoxic storm

A 
Severe hyperT
\+Temperature
Agitation
Confusion
Coma
TachY
AF, DV, goitre thyroid bruit
Acute abdomen
HF
Cardiovascular collapse
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36
Q

Precipitants of thyrotoxic storm

A

Recent thyroid surgery, radioiodine, infection, MI, trauma

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37
Q

Investigations in thyrotoxic storm

A

TSH, T4, T3, cultures, cardiac enzymes

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38
Q

What is the effect of stable iodide (Lugols, potassium iodide)

A

Acutely inhibits iodide release from thyroid in Grave’s

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39
Q

Mechanism of action of carbimazole and propylthiouracil

A

Xiodination of thyroglobulin

Xconversion T4->T3

40
Q

Side effects of thioreleyenes

A

Headache
Nausea
Rash
GIT disturbance

Most important->agranulocytosis. Monitor WCC if have sore throat/fever

41
Q

Action of guanethidine eye drops

A

adrenergic antagonist= -ve sympathetic outflow

-ve exopthalmos

42
Q

Indication, CI and mechanism for radioiodine

A

I: Mainly Relapse
CI: Pregnancy, thyroid eye disease as can worsen
M: Taken up as iodine->radiation destroys tissue

43
Q

Important side effect of radioiodine

A

Hypothyroidism

44
Q

Why is hypothyroidism +likely in Grave’s treated with radioiodine

A

++TSH= +iodine uptake

45
Q

Indications, complications of surgery

A

Obstruction, thyrotoxic, failed medical, thyroid Ca, cosmesis, eye disease (radioiodine can make worse)
Complications: recurrent/superior laryngeal nerve injury, hypoparathyroidism, hoarseness, bleeding into neck->stridor

46
Q

Definition of subacute thyroiditis

A

Acute inflammation->hyperthyroid stage->hypothyroidism->euthyroidism
Acute inflammation->release of steroid hormone, not +in production
Release of virus/thyroid antigen during infection->activation of cytotoxic T lymphocytes, damage to follicular cells

47
Q

Subtype of subacute thyroiditis

A

Painful

Painless

48
Q

Painful thyroiditis

A

DeQuervains

49
Q

Epidemiology of DQ

A

+Female

40-50 yo

50
Q

Presentation and progression of DQ

A

Post viral
Painful goiter, tender warm
Worse on movement

51
Q

Investigations in subacute thyroiditis

A

thyroid-stimulating hormone (TSH)- suppressed
total T4, total T3, T3 resin uptake, free thyroxine index - ++
T3:T4 ratio- 15:1
radioactive iodine uptake- decreased
ESR- elevated
CRP- elevated
antithyroid antibodies (thyroid peroxidase antibodies)-normal

52
Q

Why is propilthiouracil and carbimazole not useful in thyrotoxicosis associated w/ sbacute thyroiditis

A

The thyrotoxicosis associated is due to +release of thyroglobulin and not productio

53
Q

Management of hyperthyroid stage of SAT

A

Supportive
Analgesia->ibuprofen, paracetamol + codeine
If pain not controlled by NSAIDs- prednisilone
Tachy/tremor->propranolol
If severe thyrotoxicosis- potassium iodide + prednisilone

54
Q

Management of hypothyroid phase in SAT

A

Mild: observation and reassess
+/- Levothyroxine
Moderate: levothyroxine

55
Q

Explanation for antithyroid

A

MOA: blocks thyroid hormone synthesis (propylthiouracil also blocks peripheral conversion)
Ind: Grave’s, thyroid storn, short term before surgery.
Prec: Propylthiouracil preferred in first trimester pregnancy. Carbimazole may be preferred in breastfeeding. Agranulocytosis- contraindicated
Adverse effects: usually in first 8 weeks. Itch, rash (use antihistamines), NV, leucopenia, gastric discomfort
Agranulocytosis- most commonly in first 3 months. Rapid onset.
Hepatotoxicity-> +LFTs usually resolves after 2 months with continued use.

Tell your doctor immediately is develop fever,, mouth ulcers, sore throat, rash, severe fatigue, nausea, abdominal pain or jaundice.

56
Q

Types of painless subacute thyroiditis

A

Postpartum (5-10%)
Autoimmune
Lymphocytic

57
Q

Progress of postpartum

A

Thyrotoxicosis at 2-3 mo

Hypothyroid phase 4-8 months

58
Q

What can post partum thyroiditis be mistakenly diagnosed as

A

Postpartum depression

59
Q

Prognosis of SAT

A

Full recovery in most

10% permanent hypothyroid

60
Q

Main concern in simple non toxic goiter

A 
Mass effects
Dysphagia
Tracheal deviation
Pembertons sign
Stridor
61
Q

Epidemiology of simple goiter

A

Endemic->when 10% population has goiter
Sporadic in young femals
Goitrogenic foods

62
Q

Etiology and pathogenesis of multinodular toxic goiter

A

Autonomous alterations in TSH++->recurrent hyperplasia and involution of follicular cells
+Size, number and colloid->rupture, hemorrhage, scarring and calcification

Endemic, sporadic, female, older age

63
Q

Common presentation of MNG

A

Thyrotoxic features

Elderly with new onset AF

64
Q

Investigations in T MNG

A 
TSH-> suppressed
Consider
Free T4, T3- +
I-123 thyroid scan and uptake- multiple hot and cold spots
Tc99 scan
Thyroid US
Metabolic- possible hypercalcemia, LFTs
FBC- anemia or leukocytosis. Baseline propr to starting antithyroid
TPO- negative
TSH antibodies- negative
ECG- may show AF
CT neck non-contrast- may delineate goiter
65
Q

Management of T MNG in non-preg/non lactating, with/O mass effect/suspicion of Ca

A

Radioactive iodine therapy
Pre-treat with anti-thyroid->thiamazole
Second line->surgery

66
Q

Management of TMNGwhen mass effect/suspicion of cancer

A

Surgery
Pre-treat with anti-thyroid-thiamazole
If +symptoms/CV risk->propranolol

67
Q

Management of T MNG when pregnant/breastfeeding w/o mass/suspicion of Ca

A

Antithyroid drugs
?Surgery
If +symptoms, CV risk->propranolol

68
Q

Management of thyroid eye disease

A

Get specialist input
Treat thyroid abnormalities
Advise to stop smoking as worsens
Artifical tears, sunglasss, avoid dust, elevate bed when sleeping
If more severe may need steroids
Sight-threatening->surgical decompression

69
Q

Differential of diffuse goiter

A

Physiological
Grave’s
Hashimotos thyroiditis
Subacute thyroiditis

70
Q

Differential of nodular goiter

A

Multinodular goiter
Adenoma
Carcinoma

71
Q

Definition of hypothyroidism

A

Clinical syndrome caused by cellular responses to insufficient thyroid hormone

72
Q

Symptoms

A 
weakness
lethargy
cold sensitivity
constipation
weight gain
depression
menstrual irregularity
myalgia
dry or coarse skin
eyelid oedema
thick tongue
facial oedema
coarse hair
bradycardia
goitre
73
Q

Signs

A 
BRADYCARDIC
Reflexes relax slowly
Ataxia
Dry skin/hair
Yawning/drowsy/coma
Cold hands
Ascites/non-pitting edema/pericardial effusion/pleural effusion
Round/puffy face
Defeated demeanour
Immobile +/- ileus
CCF

Neuropathy, myopathy

74
Q

Etiology

A

Autoimmune:
Primary atrophic thyroiditis
Hashimotos

Other:
Post thyroidectomy/radioiodine
Drug induced-goitrogens (iodine), PTU, MMI, lithium
Infiltrative
Iodine deficiency
Congenital
Neoplasia
Subacute thyroiditis

Secondary hypothyroidism- pituitary
Tertiary- hypothalamus

Peripheral resistance- Refetoff syndrome

75
Q

Hypothyroidism associations

A 
Turners and Downs
CF
PBC
Ovarian hyperstimulation
POEM's syndrome
Dyshormonogenesis
76
Q

What is POEM’s syndrome

A

Polyneuropathy
Organomegaly
Endocrinopathy
m-protein bank

77
Q

Pregnancy problems with hypthyroidism

A 
Eclampsia
Anemia
Prematurity
Low birthweight
Stillbirth
PPH
78
Q

Subclinical hypothyroid investigation findings

A

+TSH, normal free T4

79
Q

What is hashimoto’s

A

Chronic autoimmune thyroiditis

80
Q

Two major forms of hashimoto’s

A

Goitrous

Atrophic

81
Q

What is the difference between how goitrous and strophic hashimoto’s presents

A

Goitrous->goiter and euthyroid, then progresses to hypothyroidism
Atrophic presents with hypothyroidism from the start

82
Q

What is the pathophysiology of Hashimoto’s

A

Defect in T suppressors lead to cell mediiated destruction of thyroid follicles.
B cells->autoantibodies against thyroglobulin, thyroid peroxidase, TSH receptor and Na/I symporter

83
Q

Risk factors for Hashimoto’s

A

Female
Genetic susceptibility (Down’s, Turner’s)
Family/personal history of autoimmune disease
Smoking
High iodine intake
Stress and infection

84
Q

Investigations in Hashimoto’s

A 
High TSH
Low T4
Thyroid peroxidase and thyroglobulin antibodies
\+LDL
Anemia
85
Q

What is myxedema coma

A

Severe form, untreated hypothyroidism

86
Q

Presentation of myxedema coma

A 
Impaired consciousness
Hypoventilation
Hypothermia
Hyponatremia
Hypotension
Hypoglycemia
Bradycardia
Generalised edema
87
Q

What is myxedema coma complicated by

A 
Trauma
Sepsis
Cold exposure
Administration of hypnotics/narcotic
Stressful events
88
Q

Why hyponatremia in myxedema

A

Low activity of Na/K ATPase->impaired sodium/water reabsorption

89
Q

Treatment of myxedema coma

A

ABCs, ICU
Baseline cortisol then Hydrocortisone
Thyroxine
Supportive: mechanical ventilation, fluids, vasopressor, rewarming, dextrose
ECG monitoring
Look for underlying cause and treat->infection, MI etc

Must have IV therapy b/c impaired GI motility

90
Q

Investigations in myxedema

A 
\+TSH
Low T4, T3
UEC: hyponatremia
\+Serum creatinine (reduced renal excretion)
ABG
Cultures->look for sepsis
\+Creatinine kinase
Glucose->hypoglycemia
CBC->look for infection

CXR: Cardiomegaly, pericardial effusion, congestive heart failure, and/or pleural effusion are observed.

91
Q

What is sick euthyroid syndrome

A

Transient change in thyroid hormones amoungst patients with serious illness, trauma or stress
No intrinsic thyroid/pituitary disease
Low T3, Low TSH, (if severe low T4)
With recovery TSH may overshoot and become high

92
Q

Mechanisms of SES

A

Inhibition of thyroid-releasing hormone and thyroid-stimulating hormone secretion
Abnormal thyroid binding to thyroid binding proteins
Decrease in thyroid binding globulin

93
Q

Commonest cause of thyroid mass

A

Colloid mass

Thyroid adenoma or hyperplastic nodule

94
Q

Less common cause of thyroid mass

A 
Non-toxic multinodular goitre
 Toxic adenoma, single
 Toxic multinodular goitre
 Differentiated thyroid cancer (papillary, follicular)
 Medullary thyroid cancer
 Anaplastic thyroid cancer
 Lymphoma
 Simple epithelial-lined thyroid cyst
 Thyroglossal duct cyst
 Acute suppurative thyroiditis
 Subacute granulomatous thyroiditis
 Chronic lymphocytic (Hashimoto's) thyroiditis
 Painless lymphocytic thyroiditis
 Graves' disease
 Enlarged parathyroid gland(s): benign
 Parathyroid carcinoma
 Metastasis from non-thyroidal malignancies
95
Q

Counselling the use of levothyroxine

A

Synthetic version of normal hormone
Give to bring levels up to normal
Once daily before breakfast
Tablet form
Take for life
Start test dose then review in 2-3 weeks
TSH test every 2-3 months until stable
When TSH level stable, check annually
Side effects rare when thyroxine levels stable
May have hyperthyroid symptoms-vomiting, diarrhea, HA, palpitations, heat intolerance
Safe in pregnancy- may need to increase dose

Internal Medicine (67 decks)

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